Institute of Pathology, University of Wuerzburg, Germany.
Comprehensive Cancer Center (CCC) Mainfranken Wuerzburg, Germany.
J Alzheimers Dis. 2019;67(1):149-157. doi: 10.3233/JAD-180661.
Oxidative stress is implicated in the pathogenesis of neurodegenerative diseases, including sporadic Alzheimer's disease (AD). Mitochondrial DNA (mtDNA) deletions are markers of oxidative damage with an age-dependent accumulation. In a previous study, we analyzed mtDNA levels in diverse neuronal cell types in order to unravel the impact of oxidative stress in brains of AD patients. The aim of this study was to identify possible correlations between mtDNA deletion levels of selected astrocytes and microglia from three brain regions with different vulnerability to AD pathology and different stages of disease compared to controls. Our results reflect a higher vulnerability of hippocampal astrocytes and microglia to oxidative stress compared to other brain regions, such as cerebellum and brainstem.
氧化应激与神经退行性疾病的发病机制有关，包括散发性阿尔茨海默病（AD）。线粒体 DNA（mtDNA）缺失是氧化损伤的标志物，随着年龄的增长而积累。在之前的一项研究中，我们分析了不同神经元细胞类型中的 mtDNA 水平，以揭示氧化应激对 AD 患者大脑的影响。本研究的目的是确定与 AD 病理学易感性不同的三个脑区的选定星形胶质细胞和小胶质细胞的 mtDNA 缺失水平与对照组之间的可能相关性。我们的研究结果反映了与其他脑区（如小脑和脑干）相比，海马星形胶质细胞和小胶质细胞对氧化应激的易感性更高。
